Role of the liver in the degradation of very low density lipoproteins: a study of lipolysis by heparin releasable liver lipase and uptake during isolated rat liver perfusion

Publisher Website
Google Scholar
Abstract
The role of the liver and of a heparin-releasable liver lipase in the metabolism of very low density lipoprotein (VLDL) was investigated in vitro and during recycling rat liver perfusion. Rat plasma VLDL and nascent hepatic VLDL were labeled biosynthetically in their lipid moieties. Incubation in vitro of VLDL with the lipase caused hydrolysis of VLDL-triglycerides (> 80%) and VLDL-phosphatidylcholine (> 30%). Nascent VLDL was a better substrate for the enzyme. The hydrolytic activities were inhibited by 70-90% when rat plasma (10-30 vol%) was added to the incubation mixture. VLDL-triglycerides and cholesterol esters were taken up by the liver during 180 min recycling perfusion. The rate of disappearance of nascent VLDL was faster than that of plasma VLDL. Injection of heparin into the perfusion medium caused accelerated uptake of the hydrolyzed VLDL-triglyceride by the liver. Addition of plasma to the perfusion at a concentration of 10 vol% delayed the rate of disappearance of VLDL from the perfusate by .apprx. 50-75%. The capacity of hepatic lipase to hydrolyze VLDL-lipids and the ability of the liver to degrade nascent and plasma VLDL particles were established. These 2 activities are depressed by plasma and therefore previous studies of VLDL metabolism may have to be reexamined when based on incubations or perfusions in the absence of plasma.

This publication has 40 references indexed in Scilit: